Pulmonary vascular remodeling and inflammation play an important role in the hypoxic-induced lung diseases. Our previous investigations showed that peptide from yak milk residues could alleviate inflammation. In this study, our results suggest that peptide (LV) from yak milk residues peptide had protective effect of lung in the animal models of hypoxic-induced lung injury. LV Gavage could improve pulmonary vascular remodeling in the lung tissues of hypoxic mice. A comprehensive analysis of metabolomics and transcriptomics revealed that 5-KETE, 8,9-EET, and 6-keto-prostaglandin F1a might be potential targets to prevent lung injury in the hypoxic mice. These metabolites can be regulated by MAPK/VEGF and inflammatory pathways. Our data indicated that LV treatment could inhibit apoptosis and inflammation via Nrf2/NF-κB/MAPK/PHD-2 pathway and protected hypoxic-induced lung epithelial cells injury. Taken together, our results suggest that LV provides a novel therapeutic clue for the prevention of hypoxia-induced lung injury and inflammation-related lung diseases.

中文翻译：

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牦牛活性肽通过抑制 VEGF/MAPK/炎症信号传导抑制缺氧引起的肺损伤


肺血管重塑和炎症在缺氧引起的肺部疾病中发挥重要作用。我们之前的研究表明，牦牛奶渣中的肽可以减轻炎症。在本研究中，我们的结果表明，牦牛乳残肽中的肽（LV）对缺氧性肺损伤动物模型具有肺保护作用。左心灌胃可以改善缺氧小鼠肺组织中的肺血管重塑。代谢组学和转录组学的综合分析表明，5-KETE、8,9-EET 和 6-酮前列腺素 F1a 可能是预防缺氧小鼠肺损伤的潜在靶点。这些代谢物可以通过 MAPK/VEGF 和炎症途径进行调节。我们的数据表明，LV治疗可以通过Nrf2/NF-κB/MAPK/PHD-2通路抑制细胞凋亡和炎症，并保护缺氧引起的肺上皮细胞损伤。综上所述，我们的结果表明，LV 为预防缺氧引起的肺损伤和炎症相关的肺部疾病提供了新的治疗线索。